An apparatus for unilateral spinal cord compression includes a fixed member and a movable member that moves longitudinally along the fixed member by using a linear actuating mechanism to compress a portion of spinal cord encompassed by the movable member and the fixed member.

The present invention relates to the identification of a microRNA family, designated miR-29a-c, that is a key regulator of fibrosis in cardiac tissue. The inventors show that members of the miR-29 family are down-regulated in the heart tissue in response to stress, and are up-regulated in heart tissue of mice that are resistant to both stress and fibrosis. Also provided are methods of modulating expression and activity of the miR-29 family of miRNAs as a treatment for fibrotic disease, including cardiac hypertrophy, skeletal muscle fibrosis other fibrosis related diseases and collagen loss-related disease.

This invention relates to a pharmaceutical composition for treatment of a bone disease comprising, as an active ingredient, a protein comprising an extracellular cysteine-rich domain, which is from the Frizzled receptor selected from the group consisting of mammalian animal-derived Frizzled 1, Frizzled 2, and Frizzled 7 and has activity of increasing bone mass, bone density, and/or bone strength, or a mutant of such domain having sequence identity of 85% or higher to the amino acid sequence of the domain and having activity of increasing bone mass, bone density, and/or bone strength, or a vector comprising a nucleic acid encoding the protein.

The invention relates to inhibitors of Sghrt and/or Gas5 lincRNAs, in particular to polynucleotides complementary to coding and non-coding sequences of said lincRNAs, and methods of producing said inhibitors. Also disclosed are the use of the afore agents to proliferate, regenerate or dedifferentiate a heart cell; methods for preventing and treating cardiac disease using the afore agents; and a prognostic or diagnostic assay to assess the regenerative or proliferative capacity of heart tissue before, after or during a cardiac treatment regimen, comprising determining the presence or amount of Sghrt and/or Gas5 lincRNAs. The present disclosure also relates to a method for screening for a therapeutic agent that can be used to treat or prevent a heart disorder, comprising analysing the functional expression and/or expression level of Sghrt and/or Gas5 lincRNAs in the presence and in the absence of the therapeutic agent.

The present invention relates to a pharmaceutical composition for treating macular degeneration, and more particularly to a pharmaceutical composition for treating macular degeneration, which comprises an inhibitor of mTOR gene expression. The pharmaceutical composition according to the present invention can effectively treat age-related macular degeneration, a representative retinal disease that causes blindness in adults.

A method for creating an animal model of indirect traumatic optic neuropathy, including fully exposing an internal segment of an optic canal as well as adjacent anterior skull base, posterior ethmoid sinus and lateral sphenoid sinus walls through an ethmoid sinus-sphenoid sinus operation pathway under an endoscope, and impacting different sites of the internal segment of the optic canal with controllable impact force to cause optic nerve injury so as to prepare a controllable and quantifiable ITON bionic elastic injury animal model reflecting contusion to an internal segment of an optic canal in a human ITON clinical injury state. With less intracranial combined injury to the animal, the survival rate is high. Different sites of the optic canal are impacted with quantifiable elastic force for the quantitative and qualitative purposes with respect to the injured parts and the injury degree.

A transplantation method to increase the establishment rate of human tumors in immunodeficient mice. A pocket is created in the mouse and the tumor and surrounding tissues are implanted in the pocket. The pocket is left open to oxygenate the tumor and surrounding tissues.

The present invention includes a method of treating ischemic stroke, comprising administering to a subject with ischemic stroke an FGF-1, FGF-1.sub.1-155, FGF-1.sub.1-141, or combinations thereof, in an amount sufficient to cross the blood brain barrier and reduce or eliminate the ischemic stroke. In one aspect, the method also includes administering at least one other therapeutic agent to the subject, before, concurrently with or after the FGF-1, FGF-1.sub.1-155, FGF-1.sub.1-141, or combinations thereof.

The present disclosure relates generally to the use of sphingolipid-metabolizing proteins to mitigate or minimize tissue damage resulting from injury or from disease, for example, pulmonary arterial hypertension (PAH) when the sphingolipid-metabolizing protein is delivered via expression from an Anc80 vector.

Provided herein are compositions and methods comprising non-naturally occurring nucleic acid sequences that encode biologics. Also provided are methods of utilizing the provided compositions and methods as ocular therapeutics for prevention and treatment of various diseases and conditions.